scholarly journals Parasitism of hamster trachea epithelial cells by Mycoplasma pneumoniae.

1988 ◽  
Vol 56 (3) ◽  
pp. 570-576 ◽  
Author(s):  
Y Y Chen ◽  
D C Krause
Keyword(s):  
Epithelial Cells ◽  
Mycoplasma Pneumoniae ◽  
Hamster Trachea

scholarly journals Characterization of a Mycoplasma pneumoniae hmw3 Mutant: Implications for Attachment Organelle Assembly

2002 ◽  
Vol 184 (11) ◽  
pp. 3061-3068 ◽  
Author(s):  
Melisa J. Willby ◽  
Duncan C. Krause
Keyword(s):  
Epithelial Cells ◽  
Mycoplasma Pneumoniae ◽  
Cytoskeletal Protein ◽  
Respiratory Epithelial Cells ◽  
Polar Structure ◽  
Organelle Assembly ◽  
Associated Proteins ◽  
Electron Dense Core ◽  
Respiratory Epithelial

ABSTRACT The proteins required for adherence of the pathogen Mycoplasma pneumoniae to host respiratory epithelial cells are localized to a polar structure, the attachment organelle. A number of these proteins have been characterized functionally by analysis of noncytadhering mutants, and many are components of the mycoplasma cytoskeleton. Mutations in some cytadherence-associated proteins have pleiotropic effects, including decreased stability of other proteins, loss of adherence and motility, and abnormal morphology. The function of protein HMW3, a component of the attachment organelle, has been difficult to discern due to lack of an appropriate mutant. In this paper, we report that loss of HMW3 resulted in decreased levels and more diffuse localization of cytoskeletal protein P65, subtle changes in morphology, inability to cluster the adhesin P1 consistently at the terminal organelle, reduced cytadherence, and, in some cells, an atypical electron-dense core in the attachment organelle. This phenotype suggests a role for HMW3 in the architecture and stability of the attachment organelle.

scholarly journals Mycoplasma pneumoniae carriage evades induction of protective mucosal antibodies

2021 ◽  
pp. 2100129
Author(s):  
Ruben Cornelis Anthonie de Groot ◽  
Silvia Cristina Estevão ◽  
Patrick Michael Meyer Sauteur ◽  
Aditya Perkasa ◽  
Theo Hoogenboezem ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mycoplasma Pneumoniae ◽  
Community Acquired Pneumonia ◽  
Respiratory Epithelial Cells ◽  
Specific Antibodies ◽  
Asymptomatic Carriage ◽  
Nasal Secretions ◽  
Respiratory Epithelial ◽  
Nested Case Control

Mycoplasma pneumoniae is the most common bacterial cause of pneumonia in children hospitalised for community-acquired pneumonia. Prevention of infection by vaccines may be an important strategy in the presence of emerging macrolide resistant M. pneumoniae. However, knowledge of immune responses to M. pneumoniae is limited, complicating vaccine design. We therefore studied the antibody response during M. pneumoniae infection and asymptomatic carriage.In a nested case-control study (n=80) of M. pneumoniae carriers and matched controls we observed that carriage by M. pneumoniae does not lead to a rise in either mucosal or systemic M. pneumoniae-specific antibodies, even after months of persistent carriage. We replicated this finding in a second cohort (n=69) and also found that during M. pneumoniae community-acquired pneumonia, mucosal levels of M. pneumoniae-specific IgA and IgG did increase significantly. In vitro adhesion assays revealed that high levels of M. pneumoniae-specific antibodies in nasal secretions of paediatric patients prevented the adhesion of M. pneumoniae to respiratory epithelial cells.In conclusion, our study demonstrates that M. pneumoniae-specific mucosal antibodies protect against bacterial adhesion to respiratory epithelial cells and are induced only during M. pneumoniae infection and not during asymptomatic carriage. This is strikingly different from carriage with bacteria such as Streptococcus pneumoniae where mucosal antibodies are induced by bacterial carriage.

Release of Cytokines by Human Nasal Epithelial Cells and Peripheral Blood Mononuclear Cells Infected with Mycoplasma pneumoniae

2002 ◽  
Vol 227 (5) ◽  
pp. 330-335 ◽  
Author(s):  
Mikhail Y. Kazachkov ◽  
P.C. Hu ◽  
Johnny L. Carson ◽  
Paula C. Murphy ◽  
Frederick W. Henderson ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mycoplasma Pneumoniae ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Human Nasal Epithelial Cells ◽  
Tnf Α ◽  
Blood Mononuclear Cells ◽  
Syncytial Virus

Mycoplasma pneumoniae (Mp) infection is associated with asthma exacerbation in children. We hypothesized that Mp infection may cause airway inflammation by inducing the release of cytokines by respiratory epithelial cells. The levels of chemokines interleukin-8 (IL-8) and released upon activation, normal t cell expressed and secreted (RANTES) released by nasal epithelial cell (NEC) cultures established from asthmatic and nonasthmatic children were measured by ELISA at 4, 24, 48, and 72 hr after cells were inoculated with Mp, and were compared with baseline release of these factors. The presence of MP on apical membranes of NEC after infection was confirmed by transmission electron microscopy, and adherence was shown to be inhibited by erythromycin. Mp infection did not alter NEC release of IL-8 or RANTES at any time point. In contrast, tumor necrosis factor α (TNF-α) stimulated increased IL-8 at all time points, and respiratory syncytial virus (RSV) infection stimulated RANTES release at 48 and 72 hr by NEC. These results were not significantly different between NEC from asthmatic and nonasthmatic children. As a comparison, peripheral blood mononuclear cells from normal human volunteers were also incubated with Mp and had significantly increased release of IL-2, IL-6, and TNF-α. We conclude that Mp, unlike viral pathogens such as RSV, is unlikely to directly stimulate early airway surface cytokine responses via mechanisms involving epithelial cells. We speculate that the chronic presence of mononuclear cells at the airway surface of asthmatics provides a target for Mp-triggered cytokine production.

Sign in / Sign up

Export Citation Format

Share Document